Aberrant wound healing is a common problem in both the ambulatory and bedbound geriatric population. We have been studying wound healing in both in vitro and in vivo systems in an attempt to understand how the process may be altered in aging. We have found that fibroblasts produced an increase in the EDA+ isoform of fibronectin when they become senescent in culture. A similar approach could be used to characterize changes in fibronectin as wounds heal in vivo. We have also demonstrated an increase in the ratio of collagenase to collagen mRNA in fibroblasts cultured from healthy older donors compared with healthy young donors both at basal levels and after treatment with a tumor promoting agent. In vivo this altered homeostasis may predispose older individuals to develop wounds, and impair the healing process. It suggests that fibroblasts from the skin of the older donors may express some of the characteristics of cells aged in culture. Finally, we have developed an internal standard for quantitative PCR which will allow us to characterize the specific expression of collagenase I in biopsies of human skin obtained from chronic wounds.